Abstract

Fast and slowly rising inhibitory postsynaptic currents (IPSCs, IPSCF and IPSCS) in neocortical Cajal-Retzius cells are observed. In this study, zolpidem, a benzodiazepine agonist that specifically modulates gamma-aminobutyric acid type A receptors (GABAARs) containing gamma2 subunit, was used to characterize GABAARs mediating IPSCF and IPSCS. One-hundred-nanomolar zolpidem prolonged IPSCS, increased evoked IPSCS (eIPSCS) amplitude, and decreased paired-pulse ratio (PPR) of eIPSCS. Two micromolar zolpidem prolonged both IPSCF and IPSCS, increased miniature IPSCF and eIPSCF amplitudes, increased eIPSCS amplitude but not miniature IPSCS amplitude, decreased PPR of eIPSCS, but failed to affect PPR of eIPSCF. We conclude that IPSCF are mediated by alpha2/3-containing GABAARs, which are not saturated by synaptic GABA release, whereas IPSCS are mediated by alpha1-containing and alpha2/3-containing GABAARs, which are saturated by quantal GABA release.

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